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[遗传性球形红细胞增多症患儿细小病毒诱导的再生障碍危象:造血抑制机制研究]

[Parvovirus-induced aplastic crisis in a child with hereditary spherocytosis: studies on the mechanisms of hemopoietic suppression].

作者信息

Saitoh H, Horino N, Ohie T, Sejima H, Mori C

出版信息

Rinsho Ketsueki. 1989 Mar;30(3):366-70.

PMID:2549284
Abstract

A 4 4/12-year-old girl with hereditary spherocytosis (HS) who presented with an aplastic crisis during a human parvovirus (HPV) B19 infection is reported. IgM and IgG antibodies to the HPVB19 and HPV19 DNA were detected. Each of Leu 7+, Leu 11+ and HLA-DR+ cells increased. OKT4/OKT8 ratio decreased to 0.71. In order to investigate the mechanism of aplastic crisis, we used an in vitro culture technique for erythroid and granulocyte-macrophage progenitor cells (BFU-E, CFU-E and CFU-C). The patient's HPV19 DNA-containing aplastic phase serum inhibited the formation of BFU-E, CFU-E and CFU-C. After removal of the adherent cells from the aplastic phase bone marrow, the numbers of BFU-E significantly increased. These results suggest that aplastic crisis of the patient with HS was caused by HPVB19, and that monocytes-macrophages and NK cells played an important role in the pathogenesis of aplastic crisis.

摘要

报道了一名4又4/12岁患有遗传性球形红细胞增多症(HS)的女孩,她在感染人细小病毒(HPV)B19期间出现再生障碍性危象。检测到针对HPVB19的IgM和IgG抗体以及HPV19 DNA。Leu 7+、Leu 11+和HLA-DR+细胞均增多。OKT4/OKT8比值降至0.71。为了研究再生障碍性危象的机制,我们对红系和粒-巨噬系祖细胞(BFU-E、CFU-E和CFU-C)采用了体外培养技术。患者处于含HPV19 DNA的再生障碍期血清抑制了BFU-E、CFU-E和CFU-C的形成。从再生障碍期骨髓中去除贴壁细胞后,BFU-E的数量显著增加。这些结果表明,HS患者的再生障碍性危象是由HPVB19引起的,并且单核细胞-巨噬细胞和NK细胞在再生障碍性危象的发病机制中起重要作用。

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